ArticleGenes & genomics2025
miR-214-3p inhibits LPS-induced macrophage inflammation and attenuates the progression of dry eye syndrome by regulating ferroptosis in cells.
Article in Genes & genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- MiR-125a C > T, MiR-152 C > T, MiR-938 G > A, and MiR-491 G > A single nucleotide polymorphisms and their influence on genetic susceptibility to type 2 diabetes.Genes & genomics · 2026Article
- Neuroprotective Effects of lncRNA EPB41L4A-AS1 Against Ischemic Stroke Injury Through Regulating Microglial State Transition and Ferroptosis via miR-214-3p/GPX4 Axis.Neurochemical research · 2026Article
- Platform-dependent performance of P2A and IRES linkers in multicistronic gene expression.Genes & genomics · 2026Article
- The miR-214-3p/Biology · 2026Article
- Bioinformatics and experimental analysis identify CHN2 and MEF2C as diagnostic biomarkers for tuberculosis.American journal of translational research · 2026Article
- Ferroptosis and organelle roles in dry eye.iScience · 2025Review
- The Molecular Interplay Between p53-Mediated Ferroptosis and Non-Coding RNAs in Cancer.International journal of molecular sciences · 2025Review
- MicroRNA: role in macrophage polarisation and colorectal cancer pathogenesis.Frontiers in cell and developmental biology · 2025Review
- The Mitochondrial Metabolism Gene ECH1 Was Identified as a Novel Biomarker for Diabetic Nephropathy: Using Bioinformatics Analysis and Experimental Confirmation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- miR-214-3p Promotes ox-LDL-Induced Macrophages Ferroptosis and Inflammation via GPX4.Journal of inflammation research · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundDry eye disease (DED) is an ocular illness caused by insufficient tear secretion or poor tear quality, and inflammation is a key factor in its pathogenesis. Previous studies have shown that miRNAs are important regulatory factors in DED.
objectiveThe purpose of this study was to explore the potential mechanism by which miR-214-3p influenced the DED process by regulating the macrophage inflammatory response.
methodsWe induced THP-1 cells to differentiate into M0 macrophages with 100 ng/mL phorbol-12-myristate-13-acetate (PMA) and then added 15 ng/mL lipopolysaccharide (LPS) to induce inflammation. The expression of related genes and proteins was detected via RT‒qPCR, Western blotting, ELISA and immunofluorescence staining; cell viability was measured using the CCK-8 assay; and flow cytometry was used to detect ROS levels.
resultsIn tear and serum samples from DED patients, the levels of miR-214-3p, IL-10, and Arg1 were decreased, and the levels of IL-6, TNF-α, IL-1β, and iNOS expression were increased. Moreover, the overexpression of miR-214-3p attenuated the effect of LPS and inhibited M1 polarization and inflammation in macrophages. Mechanistically, miR-214-3p inhibited macrophage ferroptosis by downregulating TFRC expression, thereby inhibiting macrophage M1 polarization and inflammation and alleviating the progression of DED.
conclusionsOur study indicated that the upregulation of miR-214-3p expression might be a new target for DED therapy.
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